There are conflicting data on whether variations in physiological cortisol levels are associated with cardiovascular risk, and it can be difficult to compare results from previous studies because of varying sample size, techniques for assessing cardiovascular risk and failure to adequately account for environmental factors.

To address these issues, Haas et al. used a large sample size, selected the Framingham risk score to compute cardiovascular risk and performed the study in a highly controlled setting. They aimed to determine whether higher cortisol levels were associated with increased cardiovascular risk and whether caveolin-1 (rs926198) risk allele carriers had increased cardiovascular risk.

This was a cross-sectional study of 574 non-diabetic individuals who completed a common protocol. Data collection included fasting blood samples, blood pressure measurements and 24-h urine free-cortisol collection. Of these participants, 517 also completed caveolin-1 genotyping. Subjects were classified as belonging to either the low-mode or high-mode urine free-cortisol groups, based on the bimodal distribution of urine free-cortisol.

In multivariate analysis, Framingham risk score was statistically higher in the high-mode cortisol group (10.22±0.43; mean±SEM) compared with the low-mode cortisol group (7.73±0.34; P<0.001). Framingham risk score was also statistically higher in the caveolin-1 risk allele carriers (8.91±0.37) compared with caveolin-1 non-risk allele carriers (7.59±0.48; P=0.034).

These data still do not prove causation and call into question any suggested intervention: should we be aiming to lower urine-free cortisol, or should we heed advice to watch our weight, BP and exercise?

Read the full article in Endocrine Connections doi:10.1530/EC-19-0182